Hibernating myocardium

Last revised by Bahman Rasuli on 14 Mar 2021

Hibernating myocardium is myocardial tissue that has reduced contractility due to poor perfusion but remains viable. In ischemic heart disease, evaluating myocardial viability is important because hibernating myocardium can recover function after revascularization. 

Hibernating myocardium is most commonly seen in the setting of chronic ischemia when myocardial cells adapt to longstanding poor perfusion by entering a state of low metabolic activity. This includes loss of myocardial contractility in the tissue affected.  This can result from progression of chronic coronary atherosclerosis or as a result of an acute ischemic event. In the later phase, it is analogous to stunned myocardium.

On myocardial perfusion imaging (Tc-99m sestamibi or Tc-99m tetrofosmin SPECT, or Rb-82 or N-13 ammonia PET), myocardial ischemia or infarct is suggested by a perfusion defect (low tracer uptake).

On F-18 FDG PET, hibernating myocardium demonstrates metabolism (tracer uptake) at levels equal or even more intense than the normal myocardium. Thus, on comparison of the two studies, hibernating myocardium is indicated by a perfusion metabolism mismatch (reduced perfusion but preserved metabolism).

On Tl-201 delayed imaging, hibernating myocardium demonstrates tracer redistribution, thus discriminating between infarction and hibernating myocardium.

On cine cardiac MRI, left ventricular myocardial ischemia or infarct is suggested by regional wall motion abnormality (hypokinesis, akinesis, or dyskinesis) or myocardial thinning (≤5.5 mm at end-diastole) 7,8.

Scar burden is then assessed by subendocardial or transmural late gadolinium enhancement. Hibernating myocardium that may improve in function or thickness after revascularization is identified by those dysfunctional or thinned regions in which hyperenhancement affects <50% wall thickness 7,8.

Viability can also be assessed using dobutamine stress MRI, wherein the contractility of hibernating (viable) myocardium improves with dobutamine stress, while nonviable myocardium remains dysfunctional.

Stress echocardiography is primarily concerned with assessment of the myocardial contractile reserve, differentiating wall motion abnormalities due to irreversible scarring from reversible defects due to critical stenosis/ischemia 6. Dobutamine stress echocardiography (DSE) involves incremental administration of the inotrope dobutamine (starting around 2.5 mcg/kg/min) while assessing wall motion with transthoracic echocardiography. Each dosage increase should be preceded by acquisition of images from the parasternal (long and short axis views) and apical (4 chamber and 2 chamber views) windows​, analyzing changes in left ventricular global and regional systolic function:

  • an increase in left ventricular function with DSE implies myocardial viability 3
    • an increase in function in at least two contiguous myocardial segments by one wall motion score grade or more required
      • left ventricular "global" viability (at least four segments improving) prognostic of significant increase in ejection fraction after revascularization
    • the highest specificity for myocardial viability achieved when a "biphasic response" occurs 6
      • describes functional improvement with low dose dobutamine and deterioration of function at higher doses
      • a "uniphasic" improvement (improved function at both low and high doses) is also suggestive
  • decrease in LV function implies irreversible loss of contractility
    • indicative of nonviable myocardium that will not respond to revascularization
    • grey scale features of scarred myocardium include;
      • decreased wall thickness (0.6 cm or less)
      • relative increase in echogenicity
  • decrease in regional deformation (strain)
    • assessed with speckle tracking echocardiography, a decrease in circumferential strain most predictive of nonviability
    • while less predictive, decreases in longitudinal and radial strain also correlate with non-viability
      • use of regional longitudinal strain, using -4.5% as a lower limit of normal, achieved a sensitivity/specificity of 81% differentiating viable from non-viable myocardium 5
  • myocardial infarction
    • matched rest and stress perfusion abnormality which does not normalize upon FDG-PET/CT. Hibernating myocardium represents a viable target for revascularization and should be distinguished from infarcted myocardium, where an attempt to revascularize would be futile.
  • myocardial ischemia: rest images will demonstrate reversal of stress perfusion abnormality.
  • stunned myocardium
    • differentiation from stunned myocardium can be difficult, but can sometimes be made on the basis of maintained or nearly maintained, perfusion with a wall motion abnormality (hibernating myocardium will have abnormal perfusion and a wall motion abnormality).
    • hibernating myocardium typically represents a chronic process whereas stunned myocardium is typically related to an acute infarction or ischemic insult resulting in altered wall motion.
    • repetitive stunning may evolve into hibernating myocardium.

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